1 INTRODUCTION
Hypertension is frequently idiopathic, with secondary causes constituting 5%–10% of cases, often due to renal, endocrine, or vascular issues[
1]. Giant hydronephrosis (GH), though uncommon, is a treatable renal etiology of hypertension, typically arising from chronic obstruction. This condition elevates intrarenal pressure, compressing renal parenchyma and impairing sodium and water excretion. Consequently, the renin-angiotensin-aldosterone system (RAAS) is activated, resulting in increased blood pressure[
2]. Timely diagnosis and treatment are crucial for alleviating hypertension and improving renal function[
3].
GH is defined as hydronephrotic sac containing over 1 L of urine, occupying the hemiabdomen, crossing the midline, or extending over five vertebral bodies[
4,
5]. While it primarily affects infants and children, most often due to ureteropelvic junction obstruction (UPJO), adults can also be affected[
6]. Other causes include stones, trauma, and tumors[
7]. Symptoms are typically vague, with abdominal swelling being common. If untreated, complications such as hypertension, renal failure, rupture, or malignant transformation may arise[
8].
We present the case of a 60-year-old woman with a decade-long history of antihypertensive treatment, who was diagnosed with GH following 2 weeks of vague abdominal pain. This case highlights the importance of considering GHs in patients with unexplained hypertension.
2 CASE PRESENTATION
A 60-year-old female patient with a 10-year history of hypertensive, treated with Telmisartan (40 mg) and Hydrochlorothiazide (12.5 mg), presented to the gastroenterology outpatient clinic with 2-week history of vague, intermittent right-sided abdominal pain. The dull, non-radiating pain had no postural or food-related triggers, was relieved by medication, and was accompanied by nausea, but not by vomiting, fever, hematuria, or dysuria. Her bladder and bowel habits were normal. She had undergone a laparoscopic cholecystectomy 12 years previously. There was no significant family history or other medical conditions.
On examination, she was afebrile with a pulse rate of 80/min and a blood pressure of 150/100 mmHg. Jugular venous pressure (JVP) was normal, and there was no pedal edema. Abdominal examination revealed a large, cystic, non-tender mass occupying almost all quadrants, with limited mobility, well-defined margins, and smooth borders (Figure 1). The rest of the systemic examination was unremarkable.
Laboratory results showed normal hematological indices, with serum creatinine at 1.07 mg/dL, blood urea nitrogen at 23 mg/dL, and normal electrolytes. Urinalysis revealed 38.4 RBCs/hpf and a negative culture. Contrast enhanced computed tomography abdomen and pelvis revealed an enlarged right kidney (19.1 cm × 15.8 cm × 14.2 cm), with significant pelvicaliectasis, thinned out parenchyma, and severely impaired renal excretion due to ureteropelvic junction obstruction UPJO (Figure 2). The dilated renal pelvis extended into the pelvic cavity, crossed the midline, and displaced the small bowel, following which she was referred to urology.
The Tc-99m ethylene dicysteine renogram revealed a non-functioning right kidney, while the left kidney functioning normally. The patient underwent a right open nephrectomy through a trans-peritoneal approach. The hydronephrotic kidney extended across the midline, and 2.5 L of hemorrhagic fluid were drained after opening Gerota's fascia (Figure 3). Nephrectomy completed and gross specimen showed a dilated pelvicalyceal system with thin parenchyma and hemorrhagic areas (Figure 4). Incidentally, postoperatively hypertension resolved, and antihypertensive was discontinued. Histopathology confirmed hydronephrosis with chronic pyelonephritis, and microscopy revealed glomerulosclerosis and thyroidization of the tubules. Blood pressure remained stable at follow-ups at the 1st and 3rd months.
3 DISCUSSION
GH, though typically seen in infants and children[
8], can occur in adults and is frequently misdiagnosed due to its resemblance to conditions like ovarian, mesenteric, pancreatic, adrenal cysts, echinococcal liver cysts, and retroperitoneal masses[
9]. Patients are often asymptomatic until the late phase, presenting with abdominal distension or vague symptoms such as nausea, constipation, dyspepsia, mild abdominal pain, or recurrent urinary infections[
10]. Rare complications include renal failure, hypertension, malignant transformation, rupture, and mechanical obstruction of nearby organs[
11].
Secondary hypertension from renal causes can arise from conditions like renal parenchymal disease, renovascular disorders (e.g., renal artery stenosis, fibromuscular dysplasia), polycystic kidney disease, renin-producing tumors, or obstructive uropathy[
12,
13]. Even unilateral hydronephrosis can trigger hypertension with contralateral kidney being normal[
14].
In GH, two key mechanisms drive hypertension: Tubuloglomerular feedback (TGF) and the renin-angiotensin-aldosterone system (RAAS). When the kidney is compressed due to hydronephrosis, the glomerular filtration rate (GFR) decreases. Reduced GFR results in reduced sodium delivery to the macula densa, which in turn triggers TGF. As a response, the afferent arterioles dilate, and renin release is stimulated. The activation of RAAS leads to sodium and water retention, thereby increasing blood volume, cardiac output, and ultimately blood pressure. While this response is initially a compensatory attempt to maintain kidney perfusion, chronic activation of TGF and RAAS can lead to sustained or persistent hypertension[
15]. Renal ischemia caused by increased renal pressure due to hydronephrosis triggers the RAAS. In this process, renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II causes vasoconstriction and stimulates the release of aldosterone, which increases sodium and water retention, further raising blood pressure[
13].
After surgical correction (via nephrectomy or obstruction correction), both TGF and RAAS can normalize, suggesting that hypertension in hydronephrosis is reversible once kidney function or the systemic effects of the impaired kidney are resolved[
16].
In certain clinical scenarios, especially when patients present with compromised renal function, urosepsis, or hemodynamic instability, percutaneous nephrostomy (PCN) can serve as an effective initial management step. It provides gradual decompression of the hydronephrotic kidney, helping to prevent complications associated with sudden decompression such as hematuria or hypotension. Moreover, PCN facilitates assessment of residual renal function prior to any definitive intervention and may be used as a temporizing or palliative measure when surgery must be delayed or is contraindicated[
8].
In summary, our unique case emphasizes the association between GH and the development of reversible hyper-reninemic hypertension[
17]. Remarkably, the hypertension resolved following nephrectomy, illustrating that addressing the underlying cause of hydronephrosis can lead to normalization of blood pressure. This case underscores the importance of early recognition and intervention in patients with hydronephrosis to prevent complications such as hypertension, which can have significant implications for long-term cardiovascular health.
4 CONCLUSION
GH resulting from UPJO is a rare yet treatable cause of secondary hypertension in adults. Its subtle and nonspecific symptoms often lead to delayed diagnosis and misdiagnosis. Maintaining a high index of suspicion for hydronephrosis in patients with unexplained hypertension is vital. Renal imaging should be utilized for early diagnosis, which can help mitigate renal complications and reduce morbidity and mortality associated with this condition.
2025 The Author(s). UroPrecision published by John Wiley & Sons Australia, Ltd on behalf of Higher Education Press.
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